The inhibitory effects of capillarisin on cell proliferation and invasion of prostate carcinoma cells |
| |
| Authors: | Ke‐Hung Tsui Ying‐Ling Chang Pei‐Shan Yang Chen‐Pang Hou Yu‐Hsiang Lin Bing‐Wei Lin Tsui‐Hsia Feng Horng‐Heng Juang |
| |
| Affiliation: | 1. Department of Urology, Chang Gung Memorial Hospital‐Linkou, Kwei‐Shan, Tao‐Yuan, Taiwan;2. Department of Traditional Chinese Medicine, College of Medicine, Chang Gung University, Kwei‐Shan, Tao‐Yuan, Taiwan;3. Graduate Institute of Traditional Chinese Medicine, College of Medicine, Chang Gung University, Kwei‐Shan, Tao‐Yuan, Taiwan;4. Graduate Institute of Clinical Medicine Science, College of Medicine, Chang Gung University, Kwei‐Shan, Tao‐Yuan, Taiwan;5. School of Nursing, College of Medicine, Chang Gung University, Kwei‐Shan, Tao‐Yuan, Taiwan;6. Department of Anatomy, College of Medicine, Chang Gung University, Kwei‐Shan, Tao‐Yuan, Taiwan |
| |
| Abstract: | Objectives Capillarisin (Cap), an active component of Artemisia capillaris root extracts, is characterized by its anti‐inflammatory, anti‐oxidant and anti‐cancer properties. Nevertheless, the functions of Cap in prostate cancer have not been fully explored. We evaluated the potential actions of Cap on the cell proliferation, migration and invasion of prostate carcinoma cells. Materials and methods Cell proliferation and cell cycle distribution were measured by water‐soluble tetrazolium‐1 and flow cytometry assays. The expression of cyclins, p21, p27, survivin, matrix metallopeptidase (MMP2 and MMP9) were assessed by immunoblotting assays. Effects of Cap on invasion and migration were determined by wound closure and matrigel transmigration assays. The constitutive and interlukin‐6 (IL‐6)‐inducible STAT3 activation of prostate carcinoma cells were determined by immunoblotting and reporter assays. Results Capillarisin inhibited androgen‐independent DU145 and androgen‐dependent LNCaP cell growth through the induction of cell cycle arrest at the G0/G1 phase by upregulating p21 and p27 while downregulating expression of cyclin D1, cyclin A and cyclin B. Cap decreased protein expression of survivin, MMP‐2, and MMP‐9 and therefore blocked the migration and invasion of DU145 cells. Cap suppressed constitutive and IL‐6‐inducible STAT3 activation in DU145 and LNCaP cells. Conclusions Our data indicate that Cap blocked cell growth by modulation of p21, p27 and cyclins. The inhibitory effects of Cap on survivin, MMP‐2, MMP‐9 and STAT3 activation may account for the suppression of invasion in prostate carcinoma cells. Our data suggest that Cap might be a therapeutic agent in treating advanced prostate cancer with constitutive STAT3 or IL‐6‐inducible STAT3 activation. |
| |
| Keywords: | |
|
|
